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Tuesday, December 17, 2013

This is a season in which we all wish one another happiness
for both Christmas and for the New Year. It is a time for happiness. However,
research into happiness does not confine itself to seasons or birthdays but
looks at overall happiness with life and, in some cases, attempts to relate
that sense of happiness to our health. For this blog, I draw on a paper
published in the Journal of Happiness Studies and no, this is not a joke, such
a journal does exist published by the Springer[1]
company and edited by Prof Antonella Dell Fave from Milan. Today’s blog centres
on a paper from the Erasmus University of Rotterdam entitled:“Healthy happiness: effects of happiness on
physical health and the consequences for preventative care[2]”.

The author begins by accepting the view that physical health
can be influenced by positive and negative mental states although this does not
suggest any role for positive mental health in prevention of serious illness
such as cancer. In this review the author focuses on longevity as a correlate
with happiness and then asks how happiness can be exploited as a concept in the
promotion of good health. In this context, happiness is defined as “overall
appreciation of one’s own life-as-a-whole” or in other words “how much one
likes the life one lives”. Such definitions of happiness allow for an objective
and universal measure of how happy people are.

The author starts with the World Database of Happiness,[3]
which shows that a positive and statistically significant correlation exists
between measures of happiness and physical health. Those for self-reported
health are greater than those correlations of happiness and health ratings
based on medical opinion. However, correlations cannot tell us anything about
cause and effect and so the author surveyed the literature in this area. Four
studies were identified where some base line measure of happiness was taken and
then health status (medically determined or self-reported) studied many years
later. In general, those results were inconclusive, which led the author to
look at measures of happiness and longevity, an objective measure of overall
health. The author recorded a total of 30 such studies, eleven of which were
among people who were in bad health. Happiness and longevity among this group
was not at all clear-cut, reinforcing the earlier point that the biological
evolution of chronic diseases, such as cancer, cannot be abated by happiness. Some
19 studies focused on health and happiness in healthy individuals. The follow
up periods ranged from 1 to 60 years with 5 covering 20 years or more.In total, some 24 effects of happiness and
health were studied of which 16 (67%) were statistically positive while in the
remaining 8 cases, a positive effect was observed which failed to reach
statistical significance. The authors conclude that the evidence clearly points
to the fact that happiness “protects” against falling ill.

This blogger would ask whether there are any overlaps between
gene profiles for longevity and gene profiles for happiness. And, “surprise, surprise”,
happiness is very highly heritable based on a large study of identical and
non-identical twins in Minnesota[4].
A basic question on wellbeing was administered to 1380 twin pairs living
together and was then re-administered to the same twins some 10 years later,
leading to the conclusion that up to 80% of the stable aspect of wellbeing is
heritable. So is it that happiness increases longevity or is it that to have
the “happiness” genes is also to have the “longevity” genes. At this point in
time we don’t know.

Happiness can influence health in many ways. Thus, it is well
known that negative mental states promote poorer immune responses, higher blood
pressure and other adverse physiological effects. In contrast, happiness is
more likely to cope with threatening information and thus less fearful of
preventative activities such as health screening. Happier people are more
likely to engage in sports and are also less likely to be fatalistic as regards
health.

Epidemiology deals with populations and tells us how our
health trajectory is determined by our many lifestyle choices. But which is
more important, health alone or happiness? Here in Ireland and I assume
elsewhere, there is understandably a huge value put on being healthy. But
happiness must over-ride health and so many individuals suffering from
life-threatening conditions daily exhibit magnificent happiness. This is beyond
the metrics of epidemiology for whom the bottom line is disease orientated. And
if we move beneath life- threatening conditions and consider the risk factors
for disease, the big paymaster of epidemiology, can we be happy and fat, or a
happy smoker or a happy hypercholesterolaemic? Of course it would be best to be
happy and healthy beyond imagination – Californian healthy even.

But that’s not life. Happiness must enter the lexicon of
those concerned with life, lifestyle and wellbeing. It is the highest level of
human achievement. And it can even be topped by also making someone else happy.

Monday, December 2, 2013

The Nobel Laureate (immunology) Sir Peter Medawar once said
that “If politics is the art of the possible, then science is the art of the
soluble” and there is no better way of solving a problem than breaking it down
to ever smaller units and then building it up again. In cell biology, this is
easy. Isolate an enzyme and study its characteristics in the test tube. Then
see what happens when an intact cell is put through its paces. Lucky cell
biologists! Studying free-living humans poses an entirely different challenge
with the boundaries of investigation set by factors ranging from ethics to
practicalities of modern day life. Notwithstanding these challenges, the study
of how the human diet influences our health must proceed with the highest
possible rigour. In certain areas we can claim tremendous success such as the
role of nutrients in neural tube defects, in age-related blindness, in blood
lipids, in blood pressure, in bone disease and the like. In obesity, we have
let ourselves down badly and nothing highlights this more than a recent
systematic review of the data on diet and obesity concluded by The Swedish
Council on Health Technology Assessment. Founded in 1987, this Council[1] is
an independent national authority, tasked by the government with assessing health
care interventions based on ‘systematic literature reviews’ of published
research.

Last week (November 27th, 2013) they launched a
report: “Diet among obese individuals”[2]. In
this instance, the data refer to those who are clinically obese with a BMI
greater than 30kg/m2. The systematic review covered all dietary
intervention studies and those observational studies that lasted at least 6
months. The review covered all known publications up to the end on May this
year. The authors used the internationally accepted GRADE[3]
system to rank the scientific quality of the data. Studies with inconsistent
results or imprecise findings/objectives or confounded by non-controlled
factors were excluded. The accepted studies were used to collectively yield a
conclusion as to the strength of the evidence linking diet to the treatment of
clinical obesity. The following ranking was used: ++++ for high quality
evidence, +++0 for moderate quality, ++00 for low quality and +000 for very low
quality evidence. The results are presented for a variety of nutritional
comparisons and then for foods.

If the document is searched for all conclusions ranked at the
highest level (++++), only three appear.They are:

·“There is
strong scientific data to indicate a link with increasing coffee intake and a
reduced risk of diabetes among obese individuals”

·“There is
strong scientific data available to indicate that initiating dietary
intervention with a VLED (very low energy diet) regimen of 8–12 weeks can
achieve greatly increased weight loss over up to 12 months for obese
individuals, but after two years the effect of the regimen is marginal”

·“There is strong scientific data available to indicate that physical
activity as a supplement to dietary intervention with energy restriction has no
significant supplementary value for weight reduction after 6 months for obese
individuals”

It is remarkable that only three conclusions
reach what would be regarded as strong evidence. The report is however large
enough for all “activists”, scientists and non-scientists, to find their own
gems in the findings. For example, the Internet is awash with claims that this
report slams low fat diets and applauds low carbohydrate diets. However, the report is quite specific about
comparisons between moderate low carbohydrate diets and low-fat diets in the
clinically obese: “There is moderately
strong scientific data to indicate that advice on moderate low carbohydrate
diets compared with advice on low fat diets for obese individuals has a more
beneficial effect on weight at 6 months. At 12 months, the effect on weight is
the same (+++0). There is inadequate data available to assess whether there is
any difference between advice on the two diets with regard to weight at 24
months (+000)”.Twist it how you
like but the facts are we have no long-term evidence on which to base such
important food and nutrition policies. The same conclusions ring through most
of the fat-carbohydrate comparisons in the report.

It is also worth looking at some of the
conclusions on foods. On “Sweet drinks” the following is one key conclusion:
“There is limited scientific data available to indicate that reduction of sweet
drinks is linked to weight loss and lower blood pressure among obese
individuals (++00)”.For “chips” the
report finds: “There is no data available to assess any effect of potatoes or
chips on body weight (no studies are available)”. For “Fruit and Vegetables”, the comments are:

·“There is limited scientific data
to indicate that advice on increased intake of fruit and vegetables, compared
with advice on reduced fat intake, leads to slightly less pronounced weight
loss at 6 months among obese individuals (++00). There is inadequate data
available to determine whether there is any difference in effect on waist size
(+000). For a longer period (12 months or more), there is inadequate data
available to determine whether advice on increased intake of fruit and
vegetables has a beneficial effect on body weight or waist size (+000).

• “There is inadequate scientific
data available to determine whether intake of fruit and vegetables demonstrates
a link with future weight change among obese individuals”.

One must bear in mind that this study was
focused on weight management in the clinically obese and that what is relevant
to that sector may not be relevant to the prevention of obesity or the
long-term treatment of moderate overweight. Nonetheless, this influential
report will serve if nothing else to show that of the 43 conclusions as regards
to the role of nutrients in the management of clinical obesity, only one single
conclusion (Very Low Energy Diets) met the top ++++ GRADE rating. Of the 51
conclusions on foods and lifestyle, two met this standard (coffee and physical
activity). How poor is that.

Monday, November 25, 2013

Globally, we are approaching a diagnostic rate for
Alzheimer’s disease of about I confirmed case per second. This will quadruple
by 2040 and by then 70% of all cases will be living in developing and emerging
economies. These are average values and although a 100% increase can be
expected on average by 2040, this will be as high as 300% in China and India.
At present, the costs of Alzheimer’s disease to society in the EU is €160
billion and that would suggest, by extrapolation, a global cost in 2040, of €
1.6 trillion. This, in today’s terms is equivalent to the combined GDP of
Ireland, New Zealand, Israel, Singapore, Sweden and Nigeria. That’s a lot of
dosh and suffering by any measure.

For many years, researchers in nutrition have been interested
in studying the link between Alzheimer’s disease and dietary patters and the
two classes of nutrients of interest have been fats, specifically a protective
role for omega-3 fats and B-vitamins, specifically a protective role for folic
acid and vitamin B12. The data in this
area are strongly supported by epidemiological studies, which use blood markers
of these nutrients and the progression on dementia. However, as I pointed out
in a previous blog (“Brain food ~ get it early” 18th of June, 2012),
when dietary intervention studies are used to verify the associations found
between diet and dementia, the outcomes have been extremely disappointing and
this, I suggested may be due to a strong link between certain genetic factors,
diet and Alzheimer’s disease.

A recent paper published in the Proceedings of the National
Academy of Sciences[1]examines
the link between B-vitamin supplementation and the destruction of grey matter
material from those parts of the brain specifically associated with Alzheimer’s
disease. An initial study was carried out over two years with 156 subjects
(mean age of 77 years) with mild cognitive impairment. Half the group received
a placebo while the other got a B-vitamin supplement (folic acid, vitamin B12
and vitamin B6). The initial study showed that whereas brain size shrank in
both groups, B-vitamin group had, overall, a reduction in the rate of shrinkage
of grey matter. This paper now moves the same research from total brain
shrinkage to the loss of grey matter specifically in those regions of the brain
associated with Alzheimer’s disease (AD) In fact, the rate of shrinkage of
AD-sensitive grey matter was 3.7% in the placebo group compared to just 0.5% in
those receiving the B-vitamin supplement.

Homocysteine is a natural part of our blood biochemistry and
high levels of homocysteine have been associated with adverse health outcomes
and, classically, low levels of plasma folic acid and vitamin B-12 lead to high
level of blood homocysteine. In this study, the authors considered the effect
of B-vitamin supplementation on individuals with initially high or low levels
of plasma homocysteine. They found that if the levels of homocysteine were
elevated at the outset, the effects of B-vitamin supplementation was amplified
among individuals with elevated homocysteine (5.2% brain loss in the placebo
group with only 0.6% loss in the B-vitamin group).

This paper doesn’t use the usual “soft” end points used to
measure cognitive decline. Instead it used structural imaging techniques of
those regions of the brain sensitive to AD atrophy as an outcome measure. This
is a very interesting finding and even a strong indication that habitual high
intakes of certain B-vitamins will reduce the rate of neuro-degeneration from mild
cognitive impairment to AD, specifically, in those subjects with high plasma
homocysteine levels. However, it isn’t definitive proof of such a link. To
begin to build of a supporting body of evidence, one would need to prove that
accelerated (rate to be defined) shrinkage (extent to be defined) of AD
sensitive regions of the brain are indeed associated with the development of
Alzheimer’s disease in subject’s with specific biochemical (such as low
homocysteine levels on blood) and genetic (gene SNP’s to be determined)
attributes. Then we would have a robust biomarker. With that established then
all manner of dietary and drug interventions could be used to study their
outcome on the biomarker and, by implication Alzheimer’s disease itself.

One thing is sure. Alzheimer’s disease, like other
neurodegenerative diseases, is likely to have a significant nutritional
dimension.

Wednesday, November 20, 2013

According to a very recent paper published in the Journal of
the American Medical Association (Pediatrics)[1],
food allergy costs a staggering $25 billion annually. This estimate was based
on a survey of 1643 caregivers of children with food allergies. These costs
are, by any measure, breath-taking. For example, in the case of obesity, for
which we have very accurate data of the true prevalence, it is estimated that
by 2030, the annual costs to the US will range somewhere between $ 48 and $66
billion[2].How on earth can childhood food allergy cost
as much as obesity? The authors break the costs down as 17% due to the direct
costs of clinical care and 83% due to hidden costs such as time off work by
parents in looking after sick children. However, the key figure in calculating
the true national cost to the US is the prevalence of food allergy, which the
authors cite as 8%. That figure was generated by the authors in an earlier
study of US children and is based on a large survey involving the carers of
over 38.000 children. Therein lies a huge problem in that the figure of 8% is
self- reported. Two recent studies have completed a systematic review and meta
analysis of the literature in this area. The first[3]
focused on the prevalence of food allergy in Europe and found that the lifetime
prevalence was 17.3 % meaning that at some point in their lives, about 1 in 6
people had encountered an allergy to food. However, the point estimate, that is
the % at a specific time, was only 5.9 %. Both these values refer to
self-reported food allergy. When food allergy diagnosis was made using a blood
test (specific IgE) the point estimate was 10.1% falling to 2.7% when the more
specific skin-prick test was applied. Importantly, when the gold standard test
of food challenge was used, the value plummeted to just 0.9%. The second study[4]
focused on allergies to plant foods and accessed data from 36 studies with over
250,000 children. The majority of studies used self-reported values for the
prevalence of food allergy. Taking fruit allergies as an example, some 21
studies using self-reporting methods found the prevalence of fruit allergy to
be as high as 6.6 % and with most studies coming in at about 1%. However, with
skin prick tests, the prevalence fell to less that 0.1%. A similar pattern was
found for vegetable and nut allergies. The authors conclude: “Prevalence
estimate of plant food allergy based on self-reported symptoms should be
treated with caution”.

A final study explored the extreme event of fatal food
allergic reactions[5].
The authors searched the literature from 1946 to 2012 and identified 13 studies
involving 165 million food allergic person years which recorded 240 fatal food
allergic reactions and 14 studies which explored such fatal events but found
none. The estimated fatality rate among allergy sufferers was 1.8 per million
person years which is less than that associated with accidental death. Peanut
allergy, which is often cited in the popular media as the most dramatic of food
allergies, had a mortality rate of 2.3 per million person years. Note that the
term “person years” refers specifically to the population who are in fact food
allergic and excludes the many who are not.

All of these data show that the popular estimates of food
allergy and its consequences are grossly inflated, as are the putative economic
costs of food allergy to carers. The true diagnosis of food allergy requires a
slow methodical approach, ultimately identified by an exclusion diet and with
the re-introduction of foods under clinical supervision. Skin prick tests are a
next level and after that the diagnostic tools range from the low reliability
ones such as blood IgE to downright quackery. For the few who are truly
allergic to foods based on a proper diagnosis, the task of avoiding the
offending food is a lifelong struggle. For the vast majority, where the
diagnosis is self-made or based on some popular quackology, the allergy is no
more than a social accessory.

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"Ever seen a fat fox ~ Human obesity explored"

About Me

I graduated from University College Dublin in 1971 with an Masters in Agricultural Chemistry, took a PhD at Sydney University in 1976 and joined the University of Southampton Medical School as a lecturer in human nutrition in 1977. In 1984 I returned to Ireland to take up a post at the Department of Clinical Medicine Trinity College Dublin and was appointed as professor of human nutrition. In 2006 I left Trinity and moved to University College Dublin as Director of the UCD Institute of Food and Health. I am a former President of the Nutrition Society and I've served on several EU and UN committees on nutrition and Health. I have published over 350+ peer reviewed scientific papers in Public Health Nutrition and Molecular Nutrition and am principal investigator on several national and EU projects (www.ucd.ie/jingo; www.food4me.org). My popular books are "Something to chew on ~ challenging controversies in human nutrition" and "Ever seen a fat fox: human obesity explored"